NAC Sustained

NAC Sustained is n-acetylcysteine, the most effective enhancer of the all-important antioxidant glutathione (GSH).

NAC Sustained is delivered in an advanced, time-released technology to maximize its effects over 8 hours. These effects include relief from the symptoms of chronic bronchitis, heavy metal chelation and the quenching of free radicals.

60 Vegi-Caps 600 mg AOR08163

SUPPLEMENT FACTS:
Serving Size: 1 Capsule

N-Acetyl-L-Cysteine ................. 600 mg

Non-medicinal ingredients: food glaze, organic sucrose, povidone, talc. Capsule: hypromellose.

AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, soy, eggs, fish or shellfish.

Suggested Use
Take one capsule twice daily with/without food, or as directed by a qualified health practitioner.

Main Applications
• Relief from the symptoms of chronic bronchitis.
• Heavy metal chelation.
• Antioxidant.
• Precursor to glutathione.
• Anti-mucus in the lungs.
• Acetaminophen overdose.
• Immune responses.
• AIDS complications.
• Anti-HIV activity in-vitro.
• Cell-protective effect when dapsone (which is cytotoxic) is used to treat Pneumocystis carinii pneumonia (PCP) in AIDS.
• Liver detoxification.

Pregnancy / Nursing
None.

Cautions
None.

N-Acetyl-L-Cysteine, or NAC, is an amino acid that acts as an antioxidant and is a precursor to glutathione (GSH). While glutathione can be described as the most important endogenously produced antioxidant in the human body, it is also a (tri)peptide, and the body has a tendency to cleave peptides into their individual units. In the case of glutathione, those individual amino acid units are glutamic acid, glycine and cysteine. Of these, cysteine is the most critical for GSH synthesis, and N-acetyl-l-cysteine is a highly efficient form of cysteine.

Therefore, while there is still a school of thought that believes supplemental glutathione can be effective, the fact remains that the most important component for the synthesis of glutathione is NAC.

NAC is also more bioavailable than glutathione and is approximately 6 times as cost-effective. However, it is in the role of glutathione precursor that NAC exerts most of its beneficial effects. These include clinical applications for:

1. Heart disease. NAC has the unique ability to inhibit levels of a specific lipoprotein called Lp(a), which is a highly advanced indicator of heart disease. In fact, Lp(a) is a much more reliable indicator than blood cholesterol levels, low density lipoprotein (HDL) levels, or the ratio of LDL to HDL.

Diets and drugs designed to lower blood cholesterol levels do not lower Lp(a) levels. Recently, it was reported that NAC is the most effective nutrient known to lower Lp(a) levels. In fact, NAC is capable of lowering Lp(a) levels by 70%. LP(a) is comprised of an LDL particle attached to the large glycoprotein apo(a) by one or more disulfide bonds. NAC breaks up the disulfide bonds by converting each disulfide group into two sulphydryl groups.

NAC also inhibits heart damage by preventing LDL from being oxidized, by reducing plasma homocysteine levels, and by free-radical quenching effects. NAC also protects against ischaemic and reperfusion damage. NAC also potentiates the coronary dilating and anti-platelet effects of nitroglycerine as well as limiting the development of tolerance to nitroglycerine. Finally, ST-depression, a clinical sign of myocardial ischemia, was not seen following pretreatment with NAC, suggesting attenuation of impaired tissue oxygenation and preservation of myocardial performance by NAC.

2. Immunity and AIDS. NAC effects immunity via its role in intracellular GSH production. This role becomes critical when normal GSH production pathways are impaired, as for example, by HIV. Research has shown that reduced intracellular GSH is the “direct and early consequence of retroviral infection”. Intracellular GSH has a powerful influence on how well T- and B-lymphocyte cells function and the production of phagocytes (macrophages, monocytes and neutrophils). NAC has been shown to block production of the AIDS virus in-vitro.

3. Detoxification & Chelation. Sulphydryl groups protect against toxins. SH groups react directly with many poisons, including herbicides, drugs (acetaminophen), environmental pollutants such as carbon tetrachloride, microorganisms including E. coli and aflatoxin, and against heavy metals. Indirectly, NAC helps with detoxification by producing optimal amounts of GSH for conjugation reactions, making harmful compounds less toxic.

NAC is approved as a drug in some European jurisdictions for use in preventing liver damage from acetaminophen overdose.

4. Respiratory effects. NAC has been used for over 30 years as a mucolytic in persons having bronchopulmonary diseases including chronic bronchitis, cystic fibrosis, asthma, sinusitis, and pneumonia. NAC helps reduce the viscosity of mucus so that it may be more easily coughed up. NAC accomplishes this by converting the disulphide bond of the mucoproteins into sulphydryl bonds and cleaving the mucoproteins into smaller molecules.

Recently, a number of studies have appeared studying the role of NAC in preventing influenza. In a 1991 Italian double-blind, placebo-controlled study of 262 patients with a susceptibility to influenza, NAC dosages of 600mg twice a day resulted in only 29% developing flu-like clinical syndrome, compared to 51% of placebo-treated subjects.

Although the body’s intestinal absorption of NAC is both rapid and almost complete, its bioavailability (the amount that actually enters the bloodstream) is quite low – approximately 4-10%. This is because the first-pass metabolism of NAC by the cells of the small intestine and liver result in the incorporation of NAC into peptide chains and the formation of a variety of metabolites.

Furthermore, NAC levels peak in the bloodstream less than one hour after oral ingestion and have a plasma half-life of approximately 2.15 hours. In order to overcome this problem, NAC’s antioxidant and cardio-protective abilities have been enhanced by its infusion to a time-released, sustained delivery system that more than triples NAC’s ability to stay in the bloodstream and prolong its benefits accordingly.

References

Flanagan, R. (1991). Use of N-Acetyl cysteine in clinical toxicology. AM.J. Med; 91: 131-9.

De Flora S, Grassi C, Carati L. (1997). Attention of influenza symptomatology and improvement of cell-mediated immunity with long-term NAC treatment. Eur. Respir J; 10: 1535-1541.

Lorber A, et al. (1973). Clinical application for heavy metal-complexing potential of N-Acetyl-cystene. J. Clin. Pharmacol; 13: 332-336.

Gavish D, Breslow JL. (1991). Lipoproteins (a) reduction by N-acetylcysteine. The Lancet; 337: 203-4.

DeCaro L, et al. Pharmacokinetics and bioavailability of oral acetylcysteine in healthy volunteers. Arzneimittelforschung. 1989 Mar;39(3):382-6.

Borgstrom L, et al. Pharmacokinetics of N-acetylcysteine in man. Eur J Clin Pharmacol 1986;31: 217-222.

Ollson B, et al. Pharmacokinetics and bioavailability of reduced and oxidized N-acetylcysteine. Eur J Clin Pharmacol 1988;34: 77-82.

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